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Gene expression profile of human epidermoid carcinoma KB cells that overexpress thymidine phosphorylase

ABSTRACT: Thymidine phosphorylase (TP) catalyzes the reversible phosphorolysis of thymidine, deoxyuridine, and their analogs to the respective bases and 2-deoxy-D-ribose-1-phosphate. TP is identical to platelet-derived endothelial cell growth factor (PD-ECGF). TP was reported to induce many angiogenic factors. However, the molecular mechanism of the TP function is still obscure. To elucidate the molecular basis for the TP function in human epidermoid carcinoma KB cells, we performed a whole genome-wide microarray analysis. Genes upregulated in KB cells overexpressing TP are supposed to represent potential molecular targets of TP in KB cells. KB cells (4 M-CM-^W 10^5) in 5 ml of culture media were cultured for 24 hours, then the growth medium was replaced with serum-free medium. These cells were maintained at 37 M-KM-^ZC in a humidified atmosphere of 5% CO2 for 12 hours, then these cells were collected for RNA extraction and quantification of the transcripts by microarray analysis.

ORGANISM(S): Homo sapiens

SUBMITTER: Sho Tabata

PROVIDER: E-GEOD-31467 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression profile of human epidermoid carcinoma KB cells that overexpress thymidine phosphorylase

Project description:Thymidine phosphorylase (TP) catalyzes the reversible phosphorolysis of thymidine, deoxyuridine, and their analogs to the respective bases and 2-deoxy-D-ribose-1-phosphate. TP is identical to platelet-derived endothelial cell growth factor (PD-ECGF). TP was reported to induce many angiogenic factors. However, the molecular mechanism of the TP function is still obscure. To elucidate the molecular basis for the TP function in human epidermoid carcinoma KB cells, we performed a whole genome-wide microarray analysis. Genes upregulated in KB cells overexpressing TP are supposed to represent potential molecular targets of TP in KB cells.

2014-08-03 | GSE31467 | GEO

5/6 nephrectomy (5/6Nx) effect on the brain

Project description:Chronic kidney disease (CKD) is a very important problem in global health treatment. CKD increases the disease risk of apoplexy, cardiac failure and cardiac infarction. In addition, neurological complications, including depression and restless legs syndrome, occur in almost all CKD patients; however, the mechanisms of these neurological complications remain unclear. Here, we showed the disruptive effect of chronic renal failure in 5/6 nephrectomy mice on an immobility time of forced swim and tail suspension test and the 24-hr rhythm of Drd2 and clock gene expressions in the striatum. These disruptive effects were induced by abnormal signal transduction in high TGF-M-NM-21 expression from the kidney. Abnormal TGF-M-NM-2 signal in the striatum led to TCF7L2 expression and ID2 induced by TCF7L2 led to disruption of the 24-hr rhythm of clock gene expression. These findings suggest that neurological complications in CKD might be overcome by amelioration of the TGF-M-NM-2 signal. Differential gene expression between 5/6 nephrectomized and sham-operated mouse was measured on the brain.

2013-08-01 | E-GEOD-35134 | biostudies-arrayexpress

5/6 nephrectomy (5/6Nx) effect on the liver

Project description:Chronic renal failure (CRF) is associated with a decrease in drug metabolism. The present study investigated the repercussions of CRF on liver cytochrome P450 (CYPs), but the mechanisms have been little explored. On the other hand, the expression of several CYP genes exhibits circadian rhythm. Here we report that downregulation of hepatic CYP3A11 (the murine homolog to human CYP3A4; the most decrease in 5/6Nx using microarray analysis) by suppressing the expression of clock gene; D-site binding protein (DBP). In vivo experiments, the mRNA levels of hepatic CYP3A11 exhibit circadian rhythm regulated by DBP and E4BP4, and significantly decreased in 5/6Nx. Microarray analysis revealed that the general transcription factors of CYP3A11 did not changed. However, DBP were downregulated and several CYP genes controlled by DBP also significantly decreased in 5/6Nx. These downregulations were not observed in angiotensin II type 1alpha receptor (AT II R1a) deficient 5/6Nx because serum TGF-betaM-BM- was not upregulate. In vitro experiments, the RNA levels of CYP3A11 and DBP were downregulated in wild-type mouse hepatocytes incubated with serum from 5/6Nx, but did not changed in Id2 (-/-) hepatocytes. In fact, hepatic Id2 was upregulated and caused the downregulation of DBP in 5/6Nx. Hepatocyte treated with SD208 (TGF-beta receptor 1 selectivity inhibitor) recovered CYP3A11, DBP and Id2 to control levels. Furthermore, 5/6Nx treated with tranilast (inhibitor of TGF-beta production or isolation) or candesartan (ARBs) also recovered CYP3A11 levels. Our findings define that DBP has effects on downregulation of CYP3A11. In CRF conditions, TGF-beta is upregulated by angiotensin II receptor in renal and downregulates DBP and CYP3A11 levels mediated by Id2 in liver. Furthermore, downregulation of CYP3A11 can prevent by tranilast or candesartan. Differential gene expression between 5/6 nephrectomized and sham-operated mouse was measured on the liver.

2013-08-01 | E-GEOD-35135 | biostudies-arrayexpress

5/6 nephrectomy (5/6Nx) effect on the brain and liver

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-08-01 | E-GEOD-35136 | biostudies-arrayexpress

Influence of G0s2 gene knockdown on primary hepatocyte

Project description:Hepatocellular carcinoma is the third leading cause of cancer death worldwide, and it is necessary to elucidate the mechanism of hepatocarcinogenesis. Circadian clock systems have been related in cell cycle and carcinogenesis. In this study, hepatocarcinogenesis induced by DEN administration in mice was inhibited by knockdown of G0s2 at early stage in carcinogenesis. In addition, the circadian expression of G0s2 in mouse liver was regulated by RARM-NM-1 controlled by clock genes and ATRA. Moreover, mice administered both ATRA and DEN were not induced hepatocellular carcinoma, and decreased the expression of G0s2 at second day after the initiation of administration. These findings suggest that the control of G0s2 expression is important in carcinogenesis and G0s2 might be the novel target for prevention, diagnosis and treatment of hepatocellular carcinoma. Differential gene expression between G0s2 siRNA or Control siRNA transfected primary hepatocyte was measured after 24 hr of transfection.

2013-08-01 | E-GEOD-39288 | biostudies-arrayexpress

The identification of differentially downregulated genes in hypoxia or G9a overexpression.

Project description:To identify that differentially downregulated genes in hypoxia or G9a overexpression, we have employed whole genome microarray expression profiling. SNU484 cells expressing GFP or GFP-G9a vector under normoxic or hypoxic conditions was used to identify that differentially downregulated genes.

2015-01-07 | E-GEOD-64710 | biostudies-arrayexpress

The Senescence-associated Secretome of Hedgehog-deficient Hepatocytes Drives MASLD Progression

Project description:The burden of senescent hepatocytes correlates with MASLD severity but mechanisms driving senescence, and how it exacerbates MASLD are poorly understood. Hepatocytes become senescent when Smoothened (Smo) is deleted to disrupt Hedgehog signaling. We aimed to determine if the secretomes of Smo-deficient hepatocytes perpetuate senescence to drive MASLD progression. RNA seq analysis confirmed that hepatocyte populations of MASLD livers are depleted of Smo(+) cells and enriched with senescent cells. When fed CDA-HFD, Smo(-) mice had lower antioxidant markers and developed worse DNA damage, senescence, MASH and liver fibrosis than Smo(+) mice. Sera and hepatocyte-conditioned medium from Smo(-) mice were depleted of thymidine phosphorylase (TP), a protein that maintains mitochondrial fitness. Treating Smo(-) hepatocytes with TP reduced senescence and lipotoxicity; inhibiting TP in Smo(+) hepatocytes had the opposite effects and exacerbated hepatocyte senescence, MASH, and fibrosis in CDA-HFD-fed mice.Therefore, we found that inhibiting Hedgehog signaling in hepatocytes promotes MASLD by suppressing hepatocyte production of proteins that prevent lipotoxicity and senescence.

2024-10-01 | GSE273523 | GEO

Effect of RIG-I activation and thymidine phosphorylase inhibition using Tipiracil on gene expression of human endothelial cells.

Project description:To investigate the role of RIG-I activation and thymidine phosphorylase inhibition human endothelial cells, we used a dsRNA agonist on HUVECs and HMVECs to activate RIG-I signaling, and further treated with tymp inhibitor TPI. We then performed differential gene expression analysis using data obtained from RNA-seq from each treatment group.

2023-05-01 | GSE204809 | GEO

Homo sapiens

Project description:Gene expression profile of human epidermoid carcinoma KB cells that overexpress thymidine phosphorylase

| PRJNA145665 | ENA

Resistance to TFT by decreased TK or overexpression of sPLA2

Project description:Trifluorothymidine (TFT) is part of the novel oral formulation TAS-102, which is currently evaluated in phase II studies. Drug resistance is an important limitation of cancer therapy. The aim of the present study was to induce resistance in the colon cancer cell line H630 using two different exposure schedules and to analyze the resistance mechanism. Cells were exposed either continuously or intermittently to TFT, resulting in H630-cTFT and H630-4TFT, respectively. Cells were analyzed for cross resistance, cell cycle, protein expression and activity of thymidine phosphorylase (TP), thymidine kinase (TK) and thymidylate synthase (TS), gene expression (microarray) and genomic alterations (array CGH). Both cell lines were cross-resistant to 2’-deoxy-5-fluorouridine (>170-fold). Exposure to IC75-TFT increased the S- and G2/M-phase of H630 cells, while in the resistant variants no change was observed. The two main target enzymes TS and TP remained unchanged in both TFT-resistant variants. In H630-4TFT cells, TK protein expression and activity were decreased, possibly related to an aberrant TK protein, clearly resulting in less activated TFT and most likely the mechanism of TFT resistance. Surprisingly, in H630-cTFT microarray analysis revealed a strong increase in mRNA levels of secretory phospholipase-A2 (sPLA2; 47-fold), which was also found by RT-PCR (211 fold increase). Inhibition of sPLA2 reversed TFT resistance partially. In addition, H630-cTFT had many chromosomal aberrations, but the exact role of sPLA2 in TFT-resistance remains unclear. Altogether, induction of resistance to TFT can lead to different mechanisms of resistance, including decreased TK protein expression and enzyme activity, as well as (phospho)lipid metabolism.

2010-06-15 | GSE18137 | GEO

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